Project C04

Project C04 studies the molecular and functional mechanisms underlying neurodegeneration-induced apraxia and its counteracting reserve mechanisms based on the hypothesis that apraxic deficits in Alzheimer’s disease (AD) are associated with the location and extent of tau-pathology in praxis-related cortical networks. Characterizing apraxia in AD at the behavioural (neuropsychological profiling, including the Cologne apraxia screening, KAS), molecular (Tau-PET imaging), and functional (resting-state fMRI) levels will provide fundamental insights into higher motor functions and may identify specific factors contributing to resilience against apraxia.